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New Advances in Molecular Research of Coronavirus
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New Advances in Molecular Research of Coronavirus

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 15 May 2024 | Viewed by 3713

Special Issue Editors

Prof. Dr. Pavel Avdonin

E-Mail Website
Guest Editor
NK Koltsov Institute of Developmental Biology RAS, Moscow 119334, Russia
Interests: COVID-19; signaling; endothelial cells
Dr. Evgeny E. Bezsonov

E-Mail Website
Guest Editor
1. Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia
2. Laboratory of Cellular and Molecular Pathology of Cardiovascular System, Avtsyn Research Institute of Human Morphology of Federal State Budgetary Scientific Institution “Petrovsky National Research Center of Surgery”, 117418 Moscow, Russia
3. Department of Biology and General Genetics, I.M. Sechenov First Moscow State Medical University (Sechenov University), 105043 Moscow, Russia
Interests: atherosclerosis; mitophagy; atherogenicity; atherosclerosis; autoantibodies; inflammation; innate immunity; amyloid
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

More than two years have passed since the start of the COVID-19 pandemic. During this time, thanks to the creation of effective vaccines, the development of new treatment protocols, the emergence of mass immunity, and the evolution of the virus towards less dangerous variants, the severity of coronavirus infection and mortality have decreased significantly; however, as a result of the mutations of SARS-CoV-2, the effectiveness of existing vaccines is reduced and the use of drugs that affect links of the pathological process, such as the interaction of the viral part with receptors and its reproduction in cells, is becoming more and more relevant. In this regard it is necessary to conduct research on the creation of new targeted drugs that inactivate SARS-CoV-2, as well as on the use of already-known drugs (drug repurposing) that can suppress the transport of viral particles into cells and neutralize the proinflammatory effect of coronavirus on the body. Despite progress in understanding the pathogenesis of COVID-19, it remains unclear as to what determines a predisposition to severe COVID-19. Further work is required to identify therapy indicators and genetic factors that can serve as prognostic signs of the development of a severe form of this disease. The canonical receptor for SARS-CoV-2 is ACE2; however, new data are emerging regarding the binding of SARS-CoV-2 onto the plasma membrane and the mechanisms of the penetration of viral particles into cells. The role of alternative SARS-CoV-2 receptors in the damage of organs and tissues of the body has not been fully elucidated. After the end of the peak phase of the pandemic, the focus in the fight against COVID-19 is shifting towards overcoming the consequences of this disease, which include musculoskeletal, digestive, and neurological symptoms, pediatric inflammatory multisystem syndrome, and disorders of the blood coagulation system as well as microcirculation. Therefore, it is important to discuss the pathogenetic mechanisms of post-COVID syndrome.

The purpose of this Special Issue is to discuss the issues raised, summarize the accumulated information, and present new data on the pathogenesis of COVID-19.

Prof. Dr. Pavel Avdonin
Dr. Evgeny E. Bezsonov
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • COVID-19

  • pathogenesis
  • SARS-CoV-2 receptors
  • drug repurposing
  • drug targets and potential treatments
  • prevention of post-COVID syndrome
  • thrombosis
  • kidney disease

Published Papers (3 papers)

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Research

13 pages, 7590 KiB  
Article
Recombinant Rod Domain of Vimentin Reduces SARS-CoV-2 Viral Replication by Blocking Spike Protein–ACE2 Interactions
by Fong Wilson Lam, Cameron August Brown and Shannon Elizabeth Ronca
Int. J. Mol. Sci. 2024, 25(5), 2477; https://doi.org/10.3390/ijms25052477 - 20 Feb 2024
Viewed by 683
Abstract
Although the SARS-CoV-2 vaccination is the primary preventive intervention, there are still few antiviral therapies available, with current drugs decreasing viral replication once the virus is intracellular. Adding novel drugs to target additional points in the viral life cycle is paramount in preventing [...] Read more.
Although the SARS-CoV-2 vaccination is the primary preventive intervention, there are still few antiviral therapies available, with current drugs decreasing viral replication once the virus is intracellular. Adding novel drugs to target additional points in the viral life cycle is paramount in preventing future pandemics. The purpose of this study was to create and test a novel protein to decrease SARS-CoV-2 replication. We created the recombinant rod domain of vimentin (rhRod) in E. coli and used biolayer interferometry to measure its affinity to the SARS-CoV-2 S1S2 spike protein and the ability to block the SARS-CoV-2–ACE2 interaction. We performed plaque assays to measure rhRod’s effect on SARS-CoV-2 replication in Vero E6 cells. Finally, we measured lung inflammation in SARS-CoV-2-exposed K18-hACE transgenic mice given intranasal and intraperitoneal rhRod. We found that rhRod has a high affinity for the S1S2 protein with a strong ability to block S1S2–ACE2 interactions. The daily addition of rhRod decreased viral replication in Vero E6 cells starting at 48 h at concentrations >1 µM. Finally, SARS-CoV-2-infected mice receiving rhRod had decreased lung inflammation compared to mock-treated animals. Based on our data, rhRod decreases SARS-CoV-2 replication in vitro and lung inflammation in vivo. Future studies will need to evaluate the protective effects of rhRod against additional viral variants and identify the optimal dosing scheme that both prevents viral replication and host lung injury. Full article
(This article belongs to the Special Issue New Advances in Molecular Research of Coronavirus)
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23 pages, 17813 KiB  
Article
Three-Dimensional Structural Stability and Local Electrostatic Potential at Point Mutations in Spike Protein of SARS-CoV-2 Coronavirus
by Svetlana H. Hristova and Alexandar M. Zhivkov
Int. J. Mol. Sci. 2024, 25(4), 2174; https://doi.org/10.3390/ijms25042174 - 11 Feb 2024
Viewed by 586
Abstract
The contagiousness of SARS-CoV-2 β-coronavirus is determined by the virus–receptor electrostatic association of its positively charged spike (S) protein with the negatively charged angiotensin converting enzyme-2 (ACE2 receptor) of the epithelial cells. If some mutations occur, the electrostatic potential on the surface of [...] Read more.
The contagiousness of SARS-CoV-2 β-coronavirus is determined by the virus–receptor electrostatic association of its positively charged spike (S) protein with the negatively charged angiotensin converting enzyme-2 (ACE2 receptor) of the epithelial cells. If some mutations occur, the electrostatic potential on the surface of the receptor-binding domain (RBD) could be altered, and the S-ACE2 association could become stronger or weaker. The aim of the current research is to investigate whether point mutations can noticeably alter the electrostatic potential on the RBD and the 3D stability of the S1-subunit of the S-protein. For this purpose, 15 mutants with different hydrophilicity and electric charge (positive, negative, or uncharged) of the substituted and substituting amino acid residues, located on the RBD at the S1-ACE2 interface, are selected, and the 3D structure of the S1-subunit is reconstructed on the base of the crystallographic structure of the S-protein of the wild-type strain and the amino acid sequence of the unfolded polypeptide chain of the mutants. Then, the Gibbs free energy of folding, isoelectric point, and pH-dependent surface electrostatic potential of the S1-subunit are computed using programs for protein electrostatics. The results show alterations in the local electrostatic potential in the vicinity of the mutant amino acid residue, which can influence the S-ACE2 association. This approach allows prediction of the relative infectivity, transmissibility, and contagiousness (at equal social immune status) of new SARS-CoV-2 mutants by reconstruction of the 3D structure of the S1-subunit and calculation of the surface electrostatic potential. Full article
(This article belongs to the Special Issue New Advances in Molecular Research of Coronavirus)
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14 pages, 2191 KiB  
Article
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Spike Protein S1 Induces Methylglyoxal-Derived Hydroimidazolone/Receptor for Advanced Glycation End Products (MG-H1/RAGE) Activation to Promote Inflammation in Human Bronchial BEAS-2B Cells
by Dominga Manfredelli, Marilena Pariano, Claudio Costantini, Alessandro Graziani, Silvia Bozza, Luigina Romani, Paolo Puccetti, Vincenzo Nicola Talesa and Cinzia Antognelli
Int. J. Mol. Sci. 2023, 24(19), 14868; https://doi.org/10.3390/ijms241914868 - 03 Oct 2023
Cited by 1 | Viewed by 1185
Abstract
The pathogenesis of coronavirus disease 2019 (COVID-19) is associated with a hyperinflammatory response. The mechanisms of SARS-CoV-2-induced inflammation are scantly known. Methylglyoxal (MG) is a glycolysis-derived byproduct endowed with a potent glycating action, leading to the formation of advanced glycation end products (AGEs), [...] Read more.
The pathogenesis of coronavirus disease 2019 (COVID-19) is associated with a hyperinflammatory response. The mechanisms of SARS-CoV-2-induced inflammation are scantly known. Methylglyoxal (MG) is a glycolysis-derived byproduct endowed with a potent glycating action, leading to the formation of advanced glycation end products (AGEs), the main one being MG-H1. MG-H1 exerts strong pro-inflammatory effects, frequently mediated by the receptor for AGEs (RAGE). Here, we investigated the involvement of the MG-H1/RAGE axis as a potential novel mechanism in SARS-CoV-2-induced inflammation by resorting to human bronchial BEAS-2B and alveolar A549 epithelial cells, expressing different levels of the ACE2 receptor (R), exposed to SARS-CoV-2 spike protein 1 (S1). Interestingly, we found in BEAS-2B cells that do not express ACE2-R that S1 exerted a pro-inflammatory action through a novel MG-H1/RAGE-based pathway. MG-H1 levels, RAGE and IL-1β expression levels in nasopharyngeal swabs from SARS-CoV-2-positive and -negative individuals, as well as glyoxalase 1 expression, the major scavenging enzyme of MG, seem to support the results obtained in vitro. Altogether, our findings reveal a novel mechanism involved in the inflammation triggered by S1, paving the way for the study of the MG-H1/RAGE inflammatory axis in SARS-CoV-2 infection as a potential therapeutic target to mitigate COVID-19-associated pathogenic inflammation. Full article
(This article belongs to the Special Issue New Advances in Molecular Research of Coronavirus)
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